Fig. 2: GluA1 CTD interactions exert a modulatory but nonessential influence on receptor synaptic anchoring.
From: AMPA receptor anchoring at CA1 synapses is determined by N-terminal domain and TARP γ8 interactions
a GluA1 CTD protein sequences with interaction mutations indicated. Dual recording of RI b and AMPAR EPSCs c from transfected and untransfected (Untrans.) cells demonstrates that PDZ-ligand mutation does not prevent full-length GluA1 synaptic anchoring in basal conditions, or in tCaMKII (tCKII)-dependent potentiation. d–e tCaMKII (tCKII) potentiation of synaptic responses is prevented by GluA1 ΔNTD, but not by GluA1 ΔNTD with a mutated PDZ-ligand (d - Dual cell Rectification Index, e Normalised AMPAR EPSC amplitudes). Prenormalised data are depicted in Supplementary Figure 3b, and data values and statistical details are presented in Supplementary Table 2. Bars represent mean values, * indicates p < 0.05, **p < 0.01, ***p < 0.001 and ns specifies no significance. Source data are provided as a source data file.
